Suppressing Nodal Signaling Activity Predisposes Ectodermal Differentiation of Epiblast Stem Cells.
IF: 7.294
Cited by: 13


The molecular mechanism underpinning the specification of the ectoderm, a transient germ-layer tissue, during mouse gastrulation was examined here in a stem cell-based model. We captured a self-renewing cell population with enhanced ectoderm potency from mouse epiblast stem cells (EpiSCs) by suppressing Nodal signaling activity. The transcriptome of the Nodal-inhibited EpiSCs resembles that of the anterior epiblast of embryonic day (E)7.0 and E7.5 mouse embryo, which is accompanied by chromatin modifications that reflect the priming of ectoderm lineage-related genes for expression. Nodal-inhibited EpiSCs show enhanced ectoderm differentiation in vitro and contribute to the neuroectoderm and the surface ectoderm in postimplantation chimeras but lose the propensity for mesendoderm differentiation in vitro and in chimeras. Our findings show that specification of the ectoderm progenitors is enhanced by the repression of Nodal signaling activity, and the ectoderm-like stem cells provide an experimental model to investigate the molecular characters of the epiblast-derived ectoderm.


Gene Expression
ectoderm propensity
epiblast stem cells
histone modification
nodal signaling

MeSH terms

Cell Differentiation
Cell Lineage
Cells, Cultured
Embryonic Development
Epigenesis, Genetic
Fluorescent Antibody Technique
Gene Expression Profiling
Gene Expression Regulation, Developmental
Germ Layers
Nodal Protein
Signal Transduction
Wnt Signaling Pathway


Liu, Chang
Wang, Ran
He, Zhisong
Osteil, Pierre
Wilkie, Emilie
Yang, Xianfa
Chen, Jun
Cui, Guizhong
Guo, Wenke
Chen, Yingying
Peng, Guangdun
Tam, Patrick P L
Jing, Naihe

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